The long term objective of this proposal is to elucidate the role of norepinephrine (NE) and beta receptors in visual system plasticity. The experiments are based on the finding that depleting NE with 6- hydroxydopamine (6-OHDA) decreases plasticity in the visual cortex. The first experiments attempt to determine whether NE depletion is sufficient for this effect. They make use of our recent finding that very small amounts of 6-OHDA can deplete NE in the visual cortex. We ask if these small doses of 6-OHDA also cause a decrease in plasticity. High performance liquid chromatography (HPLC) is used to measure NE depletion and plasticity is assayed by recording from area 17 in an animal that has had a week of monocular deprivation beginning at 5-6 weeks of age. If small, but depleting doses of 6-OHDA do not alter plasticity, we will conclude that NE depletion is not sufficient for decreases in plasticity. The next experiments ask whether NE depletion or increased beta receptor binding can better account for changes in plasticity. First, we will measure the time course of NE depletion and beta receptor binding capacity in response to 6-OHDA. Receptor binding will be measured with radioactive beta receptor ligands. Next, we will measure the dose dependence of depletion and receptor binding capacity. We ask whether the time and dose dependence of beta receptor binding better parallels changes in plasticity than does the time and dose dependence of NE depletion. The final experiments examine the role of beta receptors in the termination of the critical period. The development of beta receptors will be studied in normal, dark reared, and binocularly sutured animals. Since dark rearing but not binocular suture postpones the termination of the critical period, we hope to find that dark rearing but not binocular suture postpones the development of beta receptors.